| Method and apparatus for potentiating penile erection utilizing ultraweak electromagnetic field of very low frequency -> Monitor Keywords |
|
|
 
Method and apparatus for potentiating penile erection utilizing ultraweak electromagnetic field of very low frequencyRelated Patent Categories: Surgery, Magnetic Field Applied To Body For Therapy, Electromagnetic Coil, Pulsating FieldMethod and apparatus for potentiating penile erection utilizing ultraweak electromagnetic field of very low frequency description/claimsThe Patent Description & Claims data below is from USPTO Patent Application 20060189839, Method and apparatus for potentiating penile erection utilizing ultraweak electromagnetic field of very low frequency. Brief Patent Description - Full Patent Description - Patent Application Claims
PRIORITY CLAIM [0001] This non-provisional application claims priority from U.S. Provisional Patent Application Ser. No. 60/639,468 ("Pat. Appl. 60/639,468") filed on Dec. 28, 2004, the disclosures of which are incorporated herein by reference in their entirety. FIIELD OF THE INVENTION [0002] This invention generally relates to the use of magnetic fields to treat medical conditions. More particularly, it relates to an apparatus and method using an ultraweak, pulsed electromagnetic field of very low frequency (below 300 Hz) to potentiate penile erection. BACKGROUND OF THE INVENTION [0003] Erectile dysfunction ("ED") is defined as a persistent inability to obtain and maintain an erection satisfactory for sexual activity. Many disease states, such as diabetes, hypertension, depression, and vascular disease, are associated with this condition, which may occur many years prior to the onset of these disorders. [0004] The human penis is composed of the glans penis, the corpus spongiosum with the bulb of the penis, and the paired corpora cavernosa in which skeletal muscle structures and the continuing tunica albuginea completely surround and contain smooth muscle structures, which intermingle with fibrous tissue to form the wall of the sinusoids. The corpus spongiosum is partially entrapped by the skeletal muscle. These encased tissues finally pass through and are regulated by the surrounding structures. The penis gives the appearance of being an independent organ because of its skeletal muscle structures. They are the tissues that determine the penile shape as well as an essential part in the establishment of a rigid penis. [0005] The penis mimics the structure of other parts of the human body where skeletal muscles and the skeleton encompass those visceral organs in which smooth muscles reside. It is a pendulous organ that is uniquely suspended from the front and strongly adheres to the pubic ramus and ischium via the tenacious periostium. The organ leans on and is supported by a suspensory ligament that is an extension of the linea alba. The penis should be considered as a specialized vascular organ and an extension of the vascular system. [0006] In the penis, sinusoidal blood vessels are surrounded by a syncytium of vascular smooth muscle cells. These become dysfunctional with aging, resulting in an inability of these smooth muscle cells to relax normally following sexual stimulation. This is what primarily leads to the development of erectile dysfunction. [0007] Different types of drugs, including phosphodiesterase (PDE) inhibitors, .beta.-adrenergic receptors, and adenylate cyclase activators, have been used to treat ED, with varying degrees of success. The phenomenal success of sildenafil (Viagra.RTM.)) in improving erections in men with erectile dysfunction is due to the fact that this drug, as a phosphodiesterase inhibitor, improves the relaxation of smooth muscle cells, which become dysfunctional with the aging process. However, not everyone responds to this medication, mainly because the efficacy of the drug is directly dependent on the release of nitric oxide ("NO") from the nerve terminals of the cavernosal nerve, and this may become defective with aging or certain disease states. Many men do not respond to sildenafil and lack of efficacy is a much more common reason for discontinuation than side effects. [0008] This is further elucidated when describing the mechanism of normal erection. [0009] Erection occurs due to the relaxation of tonically constricted helicine arteries (branches of the cavernous artery) and relaxation of cavernosal smooth muscle cells (SMCs). These vasodilator events flood lacunars spaces ("sinusoids") in the paired corpora cavernosa with blood at arterial pressure. The intracavernosal pressure of the engorged penis is raised above systemic arterial pressure by the action of the ischiocavernosus muscles. The expansion of the corpora is restricted by a thick fibrous coat, the tunica albuginea, so that during erection, the venous channels draining the sinusoids are crimped, preventing venous drainage and thereby sustaining tumescence. [0010] In general, stimuli that promote penile SMCs relaxation cause erection and those that cause constriction of penile SMCs cause detumescence. As discussed in more detail below emerging evidence suggests that impairment of potassium ion ("K.sup.+") channel activity in cavernosal and arterial SMCs or reduced passive conductance of electrical signals in SMCs can lead to ED. [0011] Smooth muscle relaxation during erection depends upon the promotion of calcium ion ("Ca.sup.2+") efflux out of the smooth muscle cells. This relaxation of smooth muscle cells is mediated mainly by nitric oxide, which activates the enzyme guanylate cyclase. This cytoplasmic enzyme increases formation of the second messenger, cGMP. Elevated levels of peripheral cGMP, in turn, promote the opening of sarcolemal K.sup.+ channels inducing the efflux secondary of Ca.sup.2+ ions from the cavernosa smooth muscle cells to induce muscle relaxation, facilitate blood flow into the corpora cavernosa, and thereby help obtain, and maintain penile erection. Under physiological conditions the process of penile detumescence, mediated by efferent sympathetic pathways, follows the tumescence phase. Adrenergic sympathetic nerves release norepinephrine, which acts on adrenoceptors in penile smooth muscle. This result in reduced arterial inflow, diminished lacunar space volume and accelerated corporeal venous outflow. The flaccid state of the penis is maintained by contraction of penile smooth muscle cells mediated by the intracellular accumulation of Ca.sup.2+ ions. [0012] Despite the fact that the metabolic rate of corporal smooth muscles has not been reported yet, the penis, as an external organ, supplies a decreased temperature compared to the mean warmth of the central body (around 34.4 C. .degree.). Therefore, its energy requirements can be met at very low blood flow rates. During sexual excitement, the helicine arteries dilate and straighten which, in turn, allows blood to enter directly into the sinusoidal spaces. At that time, there is a 5-10 fold increase in blood flow to the penis, and its temperature rises one or more degrees Celsius. [0013] It is again emphasized that decreased penile vascular resistance induced by corporal smooth muscle relaxation is the most important step in penile erection. The heightened tone of the corporal smooth muscles is considered a major cause of impotence. [0014] Modulation of corporal smooth muscle tone is a complex process requiring the integration of a host of intracellular events and extracellular signals. In intracellular events of corporal smooth muscle cells, the potassium ion channels and calcium ion channels play a major role. Functionally, potassium channels are important regulators of smooth muscle membrane potential in response to depolarizing stimuli and they counteract calcium channels. Potassium channels have been shown to play a fundamental role in both the physiologic and pathophysiologic regulation of smooth muscle tone in diverse tissues. [0015] As with many other smooth muscle cell types, corporal myocyte contractility is inextricably linked to ion channel activity. Corporal smooth muscle cells possess a rich repertoire of ion channels, including calcium, chloride and potassium channels. Among these, are of particular importance, the K.sub.ATP channel (i.e., the metabolically regulated K.sup.+ channel) and the K.sub.Ca channel (i.e., the Maxi-K or large conductance, calcium-sensitive K.sup.+ channel). [0016] Ion channel functions are tied together. The opening of potassium channels will lead to the efflux of K.sup.+ down its electrochemical gradient and out of the corporal smooth muscle cell. Meanwhile, the opening of calcium channels will produce exactly the opposite effect, that is, the influx of Ca.sup.2+ down its electrochemical gradient. The former moves positive charge out of the corporal smooth muscle cell and leads to hyperpolarization (i.e., decreased membrane potential), and thus, reduced cellular excitability, primarily by virtue of the corresponding inhibition of transmembrane calcium flux through L-type voltage-dependent Ca.sup.2+ channels. [0017] The transmembrane movement of Na.sup.+, K.sup.+, Ca.sup.2+ and Cl.sup.- ions is a principal pathway by which stimuli to the extracellular membrane are transduced to the cytoplasm. Modified efflux and influx of these ions through specific plasmalemma channels will evoke changes in the membrane potential that are associated with the initiation, modulation or termination of cellular activities. [0018] Voltage-gated ion channels underlie electrical impulses in the surface membranes of excitable cells. The Na.sup.+, K.sup.+ and Ca.sup.2+ channels are all composed of homologous repeated domains that form a membrane-spanning pore. They are present in "signal" dependent organisms as low as bacteria, and as high as man. The channels are normally closed when transmembrane voltage is negative inside of the cell, relative to the extracellular space (resting state), but they open when the potential decreases or reverses. The fourth membrane-spanning segment (S4) within each domain contains positively charged residues and is thought to serve as the voltage sensor. [0019] The basic functional behavior of ion channels is based on two fundamental processes: permeation and gating. Permeation is responsible for the selective and efficient translocation of ions across the membrane, whereas gating tightly controls access of ions to the permeation pathway effectively, determining selective channel activity. Ion channels, like many other proteins, have minute moving parts that perform useful functions. Distinct formations are typically characterized by differences in the relative orientations of nearby compact domains linked by hinges or swivels ("linkers") composed of glycine residues or flexible loops. Segments are allowed rotation, and the implied rotations have direct bearing on the functional output since large orientation changes have been discovered in those minute cellular structures to allow them respond to resonant electromagnetic ("EM") pulse. Structure and Function of Certain Voltage-Gated Channels [0020] As stated, in calcium channels four homologous domains of a single polypeptide are arranged around the permeation pathway. The ion-selective permeation pathway is lined primarily by the four S6 segments and by the extracellular S5-S6 loops. The S5 and S6 segments along with the inclusive S5-S6 linker are sometimes called the pore domain of a subunit or domain. In Ca.sup.2+ channels the main voltage sensors are the four positively charged S4 segments. Each S4 segment in the Na.sup.+ and K.sup.+ channels have three to eight basic residues, either arginines or lysines, which are usually separated from each other by two neutral residues. Depolarization is expected to move S4 segments outward through the electric field. One early consequence of this S4 movement is the opening of the activation gate, believed to be formed by the cytoplasmic ends of the channel's four S6 segments, at the entrance of the permeation pathway. Prolonged depolarization also causes the inactivation of the gates by affecting openings located elsewhere in the protein to close (the "ball in the dock" is a possible mechanism). Continue reading about Method and apparatus for potentiating penile erection utilizing ultraweak electromagnetic field of very low frequency... Full patent description for Method and apparatus for potentiating penile erection utilizing ultraweak electromagnetic field of very low frequency Brief Patent Description - Full Patent Description - Patent Application Claims Click on the above for other options relating to this Method and apparatus for potentiating penile erection utilizing ultraweak electromagnetic field of very low frequency patent application. ###  How KEYWORD MONITOR works... a FREE service from FreshPatents1. Sign up (takes 30 seconds). 2. Fill in the keywords to be monitored. 3. Each week you receive an email with patent applications related to your keywords. Start now! - Receive info on patent apps like Method and apparatus for potentiating penile erection utilizing ultraweak electromagnetic field of very low frequency or other areas of interest. ### Previous Patent Application: Intraocular radiotherapy treatment Next Patent Application: Transmyocardial delivery of cardiac wall tension relief Industry Class: Surgery ### FreshPatents.com Support Thank you for viewing the Method and apparatus for potentiating penile erection utilizing ultraweak electromagnetic field of very low frequency patent info. IP-related news and info Results in 0.1998 seconds Other interesting Feshpatents.com categories: Medical: Surgery , Surgery(2) , Surgery(3) , Drug , Drug(2) , Prosthesis , Dentistry 174 |
 * Protect your Inventions * US Patent Office filing 
PATENT INFO |
|
